Myocardial infarction occurs when there is prolonged ischemia to the heart muscle due to reduced oxygen supply or increased oxygen demand. It is usually caused by formation of a blood clot within a coronary artery blocking blood flow. Diagnosis is made through symptoms, electrocardiogram changes, and cardiac biomarker levels. Treatment involves oxygen, aspirin, nitrates, beta blockers, fibrinolytics or percutaneous coronary intervention to restore blood flow, as well as long term medications like statins to prevent future heart attacks.

1. ……………………………

2. Myocardial Infarction is the rapid
development of myocardial necrosis by a
critical imbalance between oxygen supply
and demand to the myocardium

3.  Myocardial infarction result from
prolonged ischemia precipitated in most
cases by formation of occlusive thrombus
at the site of rupture of an athermatous
plaque in coronary artery.
 Rarely infarction may result from
prolonged vasospasm, inadequate
myocardial blood flow (eg hypotension) or
excessive metabolic demand.

4.  Very rarely myocardial infarction may be
caused by:
 embolic occlusion.
 Vasculitis.
 Aortic dissection.
 Aortitis.

5.  Cardiac markers in circulation indicates
myocardial infarction and help categorize MI
and is a useful adjunct to diagnosis

6.  In the US, 1.3 million cases of nonfatal MI
were reported in 2006
 Incidence of 600 per 100,000 people
 Approximately 500,000 to 700,000 deaths are
caused by heart disease annually in the
United States

7. The history is critical in making the diagnosis
of MI and sometimes provide only the only
clues that lead to the diagnosis in the initial
phase of presentation

8.  Chest Pain- anterior precordium tightness
 Pain may radiate to jaw, neck and
epigastrium
 Dyspnea- angina , poor LV function
 Nausea/abdominal pain.
 Anxiety

9.  Nausea with and without vomiting
 Diaphoresis or sweating
 Syncope or near syncope
 Elderly present with MS changes, fatigue,
syncope or weakness
 As many as half of MI are clinically silent

10.  Patient appears anxious, restless and in
distress.
 Profuse cold perspiration and pallor may
be present due to left ventricular failure.
 Patient may present with confused or
disoriented due to cerebral
hypoperfufusion.

11.  PULSE:
-Tachycardia: due to anxiety, low
cardiac output.
-Bradycardia: if there is inferior wall
infarction.
 BP: there may be hypertensive
response:>160/90.

12.  TEMPERATURE:
majority of patient with MI develop fever
within 24-48 hrs.
 RESPIRATORY RATE:
may be increased due to anxiety , pain
or heart failure.

13.  A soft first heart sound.
 Fourth heart sound.
 Systolic murmur due to papillary muscle
dysfunction .

14.  Basal crepitations mostly present .
 Crepitation may be severe involving more
than half of lung field due to left
ventricular failure.
 Diffuse wheezing may be present in
severe left ventricular failure.

15.  The physical exam can often be
unremarkable
 Hypertension
 Hypotension
 Acute valvular dysfunction may be present
 Rales
 Neck vein distention

16.  Third heart sound may be present
 A fourth heart sound poor LV compliance
 Low grade fever

17.  Most frequent cause is rupture of an
atherosclerotic lesion within coronary wall
with subsequent spasm and thrombus
formation
 Coronary artery vasospasm
 Ventricular hypertrophy
 Hypoxia
 Coronary artery emboli

18.  Cocaine
 Arteries
 Coronary anomalies
 Aortic dissection
 Pediatrics Kawasaki disease, Takayasu
arteritis
 increased myocardial demand

19.  Age
 Male gender
 Smoking
 Hypercholesterolemia and triglyceridemia
 Diabetes Mellitus
 Poorly controlled hypertension
 Type A personality

20.  Family History
 Sedentary lifestyle

21.  Acute coronary syndrome
 Anxiety
 Aortic stenosis
 Asthma
 Cholecystitis and biliary colic
 Cholethiasis
 COPD

22.  Aortic Dissection
 Endocarditis
 Esophagitis
 Shock
 Myocarditis
 Pericarditis
 Pulmonary embolism

23. The severity of an MI is dependent of three
factors
 The level of the occlusion in the coronary
 The length of time of the occlusion
 The presence or absence of collateral
circulation

24.  Cardiac biomarkers are protein molecules
released into the blood stream from
damaged heart muscle.
 Since ECG can be inconclusive ,
biomarkers are frequently used to
evaluate for myocardial injury.
 These biomarkers have a characteristic
rise and fall pattern and helps presence of
MI.

25.  These isoforms are very specific for
cardiac injury.
 Preferred markers for detecting
myocardial cell injury.
 Rise 2-6 hours after injury.
 Stay elevated for 5-14 days.

26.  Creatinine Kinase is found in heart muscle ,
skeletal muscle , and brain .
 Increased in over 90% of myocardial
infraction
 However, it can be increased in muscle
trauma, physical exertion, post-op,
convulsions, and other conditions

27.  Time sequence after myocardial infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
 MB2 released from heart muscle and
converted to MB1.
 A level of MB2 > or = 1 and a ratio of
MB2/MB1 > 1.5 indicates myocardial injury

28.  Damage to skeletal or cardiac muscle
release myoglobin into circulation.
 Time sequence after infarction
Rises fast 2hours.
Returns to normal in 20-36 hours.
 Have false positives with skeletal muscle
injury and renal failure.

29.  Diagnostic accuracy of serum markers of
cardiac injury are altered in patients with
renal failure.
 Cardiac troponins decreased diagnostic
sensitivity and specificity in patients
receiving renal replacement therapy.
 Current data show levels of troponin I are
unaltered while levels of troponin T may
be elevated during transplantation.

30.  CBC is indicated if anemia is suspected as
precipitant
 Leukocytosis may be observed within several
hours after myocardial injury and returns
returns to levels within the reference range
within one week

31.  Potassium and magnesium levels should
be monitored and corrected
 Creatinine levels must be considered
before using contrast dye for coronary
angiography.

32.  C- reactive protein is a marker of acute
inflammation
 Patients without evidence of myocardial
necrosis but with elevated CRP are at
increased risk of an event .

33.  Chest radiography may provide clues to an
alternative diagnosis ( aortic dissection or
pneumothorax)
 Chest radiography also reveals complications
of myocardial infarction such as heart failure

34.  Identifying when evaluating overall
ventricular function and wall motion
abnormalities.
 Echocardiography can also identify
complications of MI ( eg. Valvular or
pericardial effusion, VSD).

35.  A normal ECG does not exclude MI.
 High probability include ST segment
elevation in two contiguous leads or
presence of q waves on ECG.
 Intermediate probability ST depression
 T wave inversions are less specific for
diagnosis of MI.

36.  Inferior wall.
 Lateral wall.
 Anteroseptal.
 Anterolateral.
 Right ventricular.

37. The goals of therapy in AMI are
the restoration of normal
coronary flow and the maximum
recovery of functional
myocardium.

38.  Aspirin at lease 160mg immediately.
 Interferes with function of
cyclooxygenase and inhibits the formation
of thromboxane.
 Aspirin alone has one of the greatest
impact on the reduction of MI mortality.

39.  Because MI impairs the circulatory
function of the heart, oxygen by the
heart and other tissues may be
diminished.
 Supplemental oxygen should be
administered to patient with symptoms
and or signs of pulmonary edema or pulse
oximetry readings less than 90%.

40.  IV nitrates to all patients with MI and
congestive heart failure, persistent
ischemia, hypertension, or large anterior
wall MI.
 Primary benefit vasodilator effect.
 Metabolized to nitric oxide in the vascular
endothelium, relaxes endothelium.
 Vasodilatation reduces myocardial oxygen
demand .

41.  Recommended within 12 hours of MI
symptoms and continued indefinitely.
 Reduces Myocardial mortality by
decreasing death.
 Decrease the rate and force of myocardial
contraction and decreases overall oxygen
demand.

42.  Forms a chemical complex with
antithrombin III inactivates both free
thrombin and factor Xa.
 Recommended in patients with MI who
undergo surgery or fibrinolytic therapy
with has not effective.

43.  Direct activity against factors Xa and Iia.
 Proven to be effective in treating stroke
that are characterized by unstable
angina.
 Their doses are easy to administer and
laboratory testing to measure their
therapeutic effect is necessary makes
them attractive ,EG: heparin

44.  Indicated with post MI or new onset who
present less than 12 hours but not more
than 24 hours after symptom onset.
 The most critical variable in achieving
successful fibrinolysis is time form
symptom onset.

45.  As a class the plasminogen activators have
been shown to restore coronary blood
flow in 50-80% of patients
 Contraindication active:
 intracranial bleeding.
 CVA 2months.
 CNS neoplasm.
 HTN.
 coagulopathy.

46.  Retaplase slightly higher angiographic
patency but did not translate into
survival benefit.
 Intracranial bleed major risk.

47.  Potent inhibitors of platelet aggregation
 Use during PCI and in patients with high
risk features have been shown to reduce
the composite end points of death,
reinfraction.

48.  Alternative if performed by skilled operator
in an experienced center
 time of 90 minutes
 PCI can successfully restore coronary blood
flow in 90 to 95% of MI patients
 PCI definitive survival advantage for MI
patients who are in cardiogenic shock

49.  All post MI patients should be on diet ( < 7%
of calories free from saturated fats)
 MI patients with LDL > 100 mg/dl are
recommended to be on drug therapy to try to
lower levels to <100 mg/dl
 Recent data indicate that all MI patients
should be on statin therapy, regardless of
lipid levels or diet

50.  Most oral medications instituted in the
hospital at the time of MI are continued long
term
 Aspirin, beta blockers and statin are
continued indefinitely
 ACEI indefinitely in patients with CHF,
hypertension, or diabetes